PRIME International Symposium, September 28-29 2026

Chris Ponting did some commentary as well on Bluesky:

The 2026 PRIME symposium kicks off with reflections from Kelly McLellan on the importance of Patient and Public Involvement in ME/CFS research. #Prime26 #pwME #mecfs
Now up: Hannah Ollila (Helsinki) launching the new international Genetics Epidemiology of ME/CFS (GEM) consortium. Contrasting the genetics & infection trigger of narcolepsy vs #MEcfs. Narcolepsy: HLA-DQB1*06:02 carriers & autoimmunity. Talking about the importance of whole genome sequencing.
Now launches the new consortium. Its point is to identify #MEcfs pathomechanisms, susceptibility and recovery. 60,542 cases and 2.8 million controls. Well powered! Case definition: diverse info, not all optimal.
New results. Eleven associations! Focuses on EXD3 Val540Met. (NB: unpublished results that need replication.)
Genetic overlap with neuronal, immune, endocrine and sleep traits.
EXD3 missense variant in exonuclease catalytic cleft. Immune function?
Two signals in TMEM106B & VWDE locus. Associations affect gene regulation not protein sequence. Genome wide: the pituitary tissue is the most enriched in gene expression.
Is #MEcfs genetics similar to other diseases? Yes! Long Covid and fibromyalgia have strong genetic correlations w MEcfs.
 
You can really feel that this is the right direction to take ! Congratulations to them on their work. I’m really looking forward to a summary of this first day because, at the moment, it’s all a bit confusing.

There seems to be more reason for hope in half a day here than in all three days of the Stanford symposium. If only more people could channel their efforts into the momentum Ponting has set in motion.
 
You can really feel that this is the right direction to take ! Congratulations to them on their work. I’m really looking forward to a summary of this first day because, at the moment, it’s all a bit confusing.

There seems to be more reason for hope in half a day here than in all three days of the Stanford symposium. If only more people could channel their efforts into the momentum Ponting has set in motion.
I agree. I wish I could have joined but I was asleep and now have class coming up. I’m very excited to learn more and keep discussing them here!
 
My understanding, which could be wrong is that they replicated multiple (maybe 6?) of the decode hits. decodeME is also one of the cohorts included in their meta analysis.

What struck me most was they found the tissue most enriched for gene expression was the pituitary, by a wide margin over the second place tissue which was some other brain thing. I dont know exactly how they did that analysis, but it has obvious relevance to the buspirone challenge and maybe implies neuroendocrine involvement in the disease.
 
What struck me most was they found the tissue most enriched for gene expression was the pituitary, by a wide margin over the second place tissue which was some other brain thing. I dont know exactly how they did that analysis, but it has obvious relevance to the buspirone challenge and maybe implies neuroendocrine involvement in the disease.
Oh, that would be really useful for me reaching out to the pituitary people at UBC. Do we know when the pre-print will be out?
 
My understanding, which could be wrong is that they replicated multiple (maybe 6?) of the decode hits. decodeME is also one of the cohorts included in their meta analysis.

I was not able to pick up much detail. I ran through the Manhattan slide and found RABGAP. I didn't see BTN or OLFM4 but I hope you are right that several DecodeME loci held up. It sounds very likely - maybe just not the biggest peaks on the new Manhattan.

It did look different though, and it would be good if this told us more.

The study is billed as ME/CFS but I clearly heard her say that the cases all fell under a diagnosis of post-viral fatigue. That might be partly translation or local usage but I suspect not all cases were as carefully vetted as DecodeME. I think some of the DecodeME cases were not flagged as post-viral so if they went into this bigger analysis we need to clarify.

The pituitary certainly seems a new hit, but it is very closely connected to hypothalamus so hardly surprising from what we had already picked out.

Does anyone know what the other brain thingy was?
 
The study is billed as ME/CFS but I clearly heard her say that the cases all fell under a diagnosis of post-viral fatigue. That might be partly translation or local usage but I suspect not all cases were as carefully vetted as DecodeME. I think some of the DecodeME cases were not flagged as post-viral so if they went into this bigger analysis we need to clarify.

Yeah for sure i think this is inevitably
going to be the case in the non decode datasets.

The pituitary certainly seems a new hit, but it is very closely connected to hypothalamus so hardly surprising from what we had already picked out.

But the hypothalamus hasnt come out specifically as a hit anywhere before has it. I thought thag was speculation? I thought the tissue enrichment analyses were brain just in general, with eMSNs in the cell analysis.
Does anyone know what the other brain thingy was?

It may have simply been 'brain'
 
But the hypothalamus hasnt come out specifically as a hit anywhere before has it. I thought thag was speculation? I thought the tissue enrichment analyses were brain just in general, with eMSNs in the cell analysis.

You are probably right. I think we were discussing hypothalamus because it is the 'immunological window' of the brain as much as anything, together with its relation to autonomic system. I think ventral striatum came up, which is adjacent but not necessarily tightly functionally linked. Either way, an expression hit in pituitary seems consistent with lines of thought so far.
It may have simply been 'brain'
Ah, the brain brain thingy. All good, but presumably there will be some detail for us to (over)interpret in due course!
 
But the hypothalamus hasnt come out specifically as a hit anywhere before has it. I thought thag was speculation? I thought the tissue enrichment analyses were brain just in general, with eMSNs in the cell analysis.

@ME/CFS Science Blog posted an analysis of the DecodeME data where the hypothalamus came out fairly highly ranked. Sounds like this might be in the DecodeME preprint as well. (May be good to hold onto a little caution around cell-type enrichment analysis in the brain and GTEx results for now though.)
 
@ME/CFS Science Blog posted an analysis of the DecodeME data where the hypothalamus came out fairly highly ranked. Sounds like this might be in the DecodeME preprint as well.
It looks to me like that's probably mostly highlighting genes shared across many brain regions, since basically all brain regions were significant.

Interestingly, in DecodeME, pituitary was the one brain region that was not significant in the MAGMA analysis.
 
I was not able to pick up much detail. I ran through the Manhattan slide and found RABGAP. I didn't see BTN or OLFM4 but I hope you are right that several DecodeME loci held up. It sounds very likely - maybe just not the biggest peaks on the new Manhattan.

It did look different though, and it would be good if this told us more.

The study is billed as ME/CFS but I clearly heard her say that the cases all fell under a diagnosis of post-viral fatigue. That might be partly translation or local usage but I suspect not all cases were as carefully vetted as DecodeME. I think some of the DecodeME cases were not flagged as post-viral so if they went into this bigger analysis we need to clarify.

The pituitary certainly seems a new hit, but it is very closely connected to hypothalamus so hardly surprising from what we had already picked out.

Does anyone know what the other brain thingy was?
Would pituitary impacts play into the twin incidence peaks ?
 
Would pituitary impacts play into the twin incidence peaks ?
I have a feeling that it could, though at this point, anything can. My hunch would be something to do with sex hormones and how they change throughout our lives. My interest in that is driven by the buspirone-prolactin test as estradiol has a role in moderating prolactin release. However, our blood levels of estradiol are not different from healthy controls, so it's probably a bit more complicated
 
Danny Altmann seems to be admitting that all his favourite theories are not going to explain things.

He says "We have spent so many millions of pounds on all these damned autoantigen arrays."

He quotes Iwasaki's mice but is not convinced.

"So not black and white and not clear" he says.

His answer is that everything is more complicated.

Maybe it is simpler. The hypotheses were wrong?
 
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